Systematic review of Late Jurassic sauropods from the Museu Geológico collections (Lisboa, Portugal)

The Museu Geológico collections house some of the first sauropod references of the Lusitanian Basin Upper Jurassic record, including the Lourinhasaurus alenquerensis and Lusotitan atalaiensis lectotypes, previously considered as new species of the Apatosaurus and Brachiosaurus genera, respectively. Several fragmentary specimens have been classical referred to those taxa, but the most part of these systematic attributions are not supported herein, excluding a caudal vertebra from Maceira (MG 8804) considered as cf. Lusotitan atalaiensis. From the material housed in the Museu Geológico were identified basal eusauropods (indeterminate eusauropods and turiasaurs) and neosauropods (indeterminate neosauropods, diplodods and camarasaurids and basal titanosauriforms). Middle caudal vertebrae with lateral fossae, ventral hollow border by pronounced ventrolateral crests and quadrangular cross-section suggest for the presence of diplodocine diplodocids in north area of the Lusitanian Basin Central Sector during the Late Jurassic. A humerus collected from Praia dos Frades (MG 4976) is attributed to cf. Duriatitan humerocristatus suggesting the presence of shared sauropod forms between the Portugal and United Kingdom during the Late Jurassic. Duriatitan is an indeterminate member of Eusauropoda and the discovery of new material in both territories is necessary to confirm this systematic approach. The studied material is in according with the previous recorded paleobiodiversity for the sauropod clade during the Portuguese Late Jurassic, which includes basal eusauropods (including turiasaurs), diplodocids and macronarians (including camarasaurids and basal titanosauriforms).

Anabolic resistance does not explain sarcopenia in patients with type 2 diabetes mellitus, compared with healthy controls, despite reduced mTOR pathway activity

Background Ageing and type 2 diabetes mellitus (T2DM) are risk factors for skeletal muscle loss. We investigated whether anabolic resistance to feeding might underlie accelerated muscle loss in older people with T2DM and whether dysregulated mTOR signalling was implicated. Subjects 8 obese men with T2DM, and 12 age-matched controls were studied (age 68±3 vs. 68±6y; BMI: 30±2 vs. 27±5 kg·m-2). Methods Body composition was measured by dual-X-ray absorptiometry. Insulin and glucose were clamped at post-absorptive concentrations (13±2 vs. 9±3 mU·l-1; 7.4±1.9 vs. 4.6±0.4 mmol·l-1; T2DM vs. controls). Fractional synthetic rates (FSR) of myofibrillar and sarcoplasmic proteins were measured as the rate of incorporation of [13C] leucine during a primed, constant infusion of [1-13C] α-ketoisocaproic acid, 3 h after 10 or 20g of essential amino acids (EAA) were orally administered. Protein expression of total and phosphorylated mTOR signalling proteins was determined by Western blot analysis. Results Despite a significantly lower appendicular lean mass index and a greater fat mass index in T2DM vs. controls, basal myofibrillar and sarcoplasmic and post-prandial myofibrillar FSR were similar. After 20g EAA, stimulation of sarcoplasmic FSR was slightly blunted in T2DM patients. Furthermore, feeding 20g EAA increased phosphorylation of mTOR, p70S6k and 4E-BP1 by 60-100% in controls with no response observed in T2DM. Conclusions There was clear dissociation between changes in mTOR signalling versus changes in protein synthesis rates. However, the intact anabolic response of myofibrillar FSR to feeding in both groups suggests anabolic resistance may not explain accelerated muscle loss in T2DM.